ArticleComputational and structural biotechnology journal2014
Interplay Between Lipid Modulators of Kir2 Channels: Cholesterol and PIP2.
Article in Computational and structural biotechnology journal, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 27 citations in OpenAlex.
- Cholesterol Depletion with U18666A and Methyl-β Cyclodextrin Increased Small Molecule Permeability Across Brain Microvascular Endothelial Cells.Annals of biomedical engineering · 2025Article
- Article
- From Crosstalk to Synergism: The Combined Effect of Cholesterol and PI(4,5)PAdvances in experimental medicine and biology · 2023Review
- PI(4,5)PAdvances in experimental medicine and biology · 2023Article
- Phosphatidylinositol 4,5-Bisphosphate and Cholesterol Regulators of the Calcium-Activated Chloride Channels TMEM16A and TMEM16B.Advances in experimental medicine and biology · 2023Article
- Cholesterol and PIPAdvances in experimental medicine and biology · 2023Article
- Cholesterol-induced suppression of Kir2 channels is mediated by decoupling at the inter-subunit interfaces.iScience · 2022Article
- Inward Rectifier Potassium Channels: Membrane Lipid-Dependent Mechanosensitive Gates in Brain Vascular Cells.Frontiers in cardiovascular medicine · 2022Review
- Targeting Lipid-Ion Channel Interactions in Cardiovascular Disease.Frontiers in cardiovascular medicine · 2022Article
- Inwardly Rectifying Potassium Channel Kir2.1 and its "Kir-ious" Regulation by Protein Trafficking and Roles in Development and Disease.Frontiers in cell and developmental biology · 2021Review
- Defining how multiple lipid species interact with inward rectifier potassium (Kir2) channels.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Dopamine Triggers the Maturation of Striatal Spiny Projection Neuron Excitability during a Critical Period.Neuron · 2018Article
- Hypercholesterolemia-Induced Loss of Flow-Induced Vasodilation and Lesion Formation in Apolipoprotein E-Deficient Mice Critically Depend on Inwardly Rectifying KJournal of the American Heart Association · 2018Article
- Phosphatidylinositol 4,5-bisphosphate, cholesterol, and fatty acids modulate the calcium-activated chloride channel TMEM16A (ANO1).Biochimica et biophysica acta. Molecular and cell biology of lipids · 2018Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
We have shown earlier that Kir2 channels are suppressed by the elevation of membrane cholesterol. Moreover, it is also well known that activation of Kir channels is critically dependent on a regulatory phospholipid, phosphatidylinositol-4,5-bisphosphate (PIP2). In this study we examined the cross-talk between cholesterol and PIP2 in the regulation of Kir2 channels. The strength of Kir2-PIP2 interactions was assessed by acute sequestering of PIP2 with neomycin dialyzed into cells through a patch pipette while simultaneously recording whole cell currents. Consistent with a reduction in PIP2 levels, dialysis of neomycin resulted in a decrease in Kir2.1 and Kir2.3 current amplitudes (current rundown), however, this effect was significantly delayed by cholesterol depletion for both types of channels suggesting that cholesterol depletion strengthens the interaction between Kir2 channels and PIP2. Furthermore, mutation of Kir2.1 that renders the channels' cholesterol insensitive abrogated cholesterol depletion-induced delay in the current rundown whereas reverse mutation in Kir2.3 has the opposite effect. These observations provide further support for the functional cross-talk between cholesterol and PIP2 in regulating Kir2 channels. Consistent with these observations, there is a significant structural overlap between cytosolic residues that are critical for the sensitivity of Kir2 channels to the two lipid modulators but based on recent studies, there is little or no overlap between cholesterol and PIP2 binding sites. Taken together, these observations suggest that cholesterol and PIP2 regulate the channels through distinct binding sites but that the signals generated by the binding of the two modulators converge.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.